孔衛(wèi)國
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·診治分析·
前庭陣發(fā)癥的臨床特征及其誤診原因分析
孔衛(wèi)國
目的分析前庭陣發(fā)癥的臨床特征及其誤診原因。方法選取2012年1月—2015年8月宣城市人民醫(yī)院門診及住院患者中最終確診為前庭陣發(fā)癥的患者11例,回顧性分析其臨床資料,總結(jié)其臨床特征及誤診原因。結(jié)果(1)臨床癥狀:發(fā)作性眩暈、頭暈10例,耳鳴4例,步態(tài)不穩(wěn)3例,聽力減退2例;伴惡心、嘔吐、上腹部不適癥狀10例。自述癥狀持續(xù)時間:6例患者癥狀持續(xù)時間<10 min,3例患者癥狀持續(xù)時間為10 min~1 h,2例患者癥狀持續(xù)時間>1 h。癥狀發(fā)作頻率:10~50次/月。發(fā)作時體格檢查:眼震11例,以水平眼震為主,無其他神經(jīng)系統(tǒng)異常體征。磁共振檢查:前庭蝸神經(jīng)與血管交互壓迫6例。電測聽檢查:聽力減退5例,其中單耳聽力減退4例,雙耳聽力減退1例;輕度減退3例,明顯減退2例。腦干聽覺誘發(fā)電位(BAEP)檢查:Ⅰ~Ⅲ波峰間期延長6例。(2)診治及誤診情況:11例患者入院后首次診斷為良性陣發(fā)性位置性眩暈(BPPV)者5例,予以手法復(fù)位治療;首次診斷為焦慮狀態(tài)2例,予以抗焦慮治療;首次診斷為后循環(huán)缺血(PCI)、腦供血不足各1例,予以預(yù)防卒中、改善循環(huán)治療;首次診斷為突發(fā)性耳聾1例,予以擴張血管、營養(yǎng)神經(jīng)治療;首次診斷為梅尼埃病1例,予以脫水、營養(yǎng)神經(jīng)治療。首次診斷至最終明確診斷為前庭陣發(fā)癥時間為3~10 d,平均(7.2±2.1)d。3例患者依據(jù)臨床癥狀、實驗室檢查明確診斷,其余8例患者均在抗癲癇藥物治療有效后結(jié)合病史明確診斷;11例患者經(jīng)治療后臨床癥狀均有不同程度緩解。結(jié)論前庭陣發(fā)癥的臨床癥狀以發(fā)作性眩暈、頭暈為主,磁共振檢查多顯示前庭蝸神經(jīng)與血管交互壓迫,BAEP檢查結(jié)果多顯示Ⅰ~Ⅲ波峰間期延長;前庭陣發(fā)癥的臨床誤診率較高的原因與臨床醫(yī)生認識不足、患者病史提供不準確、臨床癥狀缺乏特異性及缺少特異性實驗室檢查手段有關(guān)。
前庭疾?。谎?;誤診
孔衛(wèi)國.前庭陣發(fā)癥的臨床特征及其誤診原因分析[J].實用心腦肺血管病雜志,2016,24(2):106-108.[www.syxnf.net]
Kong WG.Clinical features and causes of misdiagnosis of vestibular paroxysmia[J].Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease,2016,24(2):106-108.
前庭陣發(fā)癥(vestibular paroxysmia)最早于1975年由Jannetta醫(yī)生首次發(fā)現(xiàn)[1],于1994年被正式命名并確定診斷標(biāo)準[2]。前庭陣發(fā)癥發(fā)病率較低,且缺乏特異性臨床癥狀,又無明確的實驗室檢查以明確診斷,因此導(dǎo)致該病的確診較困難,誤診率較高。本文對宣城市人民醫(yī)院門診及住院患者中最終確診為前庭陣發(fā)癥的患者進行臨床特征及其誤診原因分析,以期為前庭陣發(fā)癥的早期診斷和治療提供資料參考,現(xiàn)報道如下。
1.1一般資料選取2012年1月—2015年8月宣城市人民醫(yī)院門診及住院患者中最終確診為前庭陣發(fā)癥的患者11例,其中男4例,女7例;年齡25~70歲,平均年齡(49.2±13.0)歲。
1.2診斷標(biāo)準參照2008年Hüfner等[3]提出的前庭陣發(fā)癥的診斷標(biāo)準,具體如下:至少發(fā)生5次眩暈,且發(fā)作時具有以下特點:(1)未經(jīng)治療,眩暈發(fā)作持續(xù)數(shù)秒至數(shù)分鐘;(2)眩暈在靜息時或某種體位時發(fā)作;(3)眩暈發(fā)作時至少具備以下1項:①無伴隨癥狀,②姿勢不穩(wěn),③步態(tài)不穩(wěn),④單側(cè)耳鳴,⑤單側(cè)耳悶或耳周麻木感,⑥單側(cè)聽力下降;(4)以下項目至少具備1項:①橋小腦角區(qū)磁共振成像(MRI)平掃提示神經(jīng)血管交互壓迫,②過度換氣試驗誘發(fā)眼震,③眼震電圖發(fā)現(xiàn)前庭功能不足加重,④抗癲癇藥物治療有效;(5)排除其他疾病或無法應(yīng)用其他疾病解釋上述癥狀。
1.3方法回顧性分析患者的臨床資料?;颊呷朐汉缶M行問診、體格檢查;均完成1.5T MRI+磁共振血管造影(MRA)檢查,觀察是否存在前庭蝸神經(jīng)與血管交互壓迫;均完善純音電測聽儀和腦干聽覺誘發(fā)電位(BAEP)檢查,觀察是否存在聽力改變和BAEP異常。明確診斷后均使用抗癲癇藥物(卡馬西平、奧卡西平)治療,并觀察藥物治療效果。
2.1臨床特征臨床癥狀:發(fā)作性眩暈、頭暈10例,耳鳴4例,步態(tài)不穩(wěn)3例,聽力減退2例;伴惡心、嘔吐、上腹部不適癥狀10例。自述癥狀持續(xù)時間:6例患者持續(xù)時間<10 min,3例患者持續(xù)時間為10 min~1 h,2例患者持續(xù)時間>1 h(癥狀持續(xù)時間均為患者自述,可能不準確)。癥狀發(fā)作頻率:10~50次/月。發(fā)作時體格檢查:眼震11例,以水平眼震為主,無其他神經(jīng)系統(tǒng)異常體征。磁共振檢查:前庭蝸神經(jīng)與血管交互壓迫6例。電測聽檢查:聽力減退5例,其中單耳聽力減退4例,雙耳聽力減退1例;輕度減退3例,明顯減退2例。BAEP檢查:Ⅰ~Ⅲ波峰間期延長6例。具體見表1。
表1 11例前庭陣發(fā)癥患者臨床特征
注:體位“+”表示體位變化誘發(fā)癥狀,“-”表示體位變化不誘發(fā)癥狀;磁共振“+”表示前庭蝸神經(jīng)與血管交互壓迫,“-”表示無前庭蝸神經(jīng)與血管交互壓迫;電測聽“+”表示出現(xiàn)聽力減退,“-”表示未出現(xiàn)聽力減退;BAEP“+”表示發(fā)現(xiàn)異常,“-”表示未發(fā)現(xiàn)異常;BAEP=腦干聽覺神經(jīng)誘發(fā)電位,BPPV=良性陣發(fā)性位置性眩暈,PCI=后循環(huán)缺血
2.2診治及誤診情況11例患者入院后首次診斷為良性陣發(fā)性位置性眩暈(BPPV)5例,予以手法復(fù)位治療;首次診斷為焦慮狀態(tài)2例,予以抗焦慮治療;首次診斷為后循環(huán)缺血(PCI)、腦供血不足各1例,予以預(yù)防卒中、改善循環(huán)治療;首次診斷為突發(fā)性耳聾1例,予以擴張血管、營養(yǎng)神經(jīng)治療;首次診斷為梅尼埃病1例,予以脫水、營養(yǎng)神經(jīng)治療。首次診斷至最終明確診斷前庭陣發(fā)癥時間為3~10 d,平均(7.2±2.1)d。3例患者依據(jù)臨床癥狀、實驗室檢查明確診斷,其余8例患者均在抗癲癇藥物(卡馬西平、奧卡西平)治療有效后結(jié)合病史明確診斷;11例患者經(jīng)治療后臨床癥狀均有不同程度緩解。
眩暈是臨床常見癥狀,常見病因有BPPV、梅尼埃病、前庭神經(jīng)炎、PCI、精神性眩暈等,其中前庭陣發(fā)癥相對少見。有調(diào)查研究顯示,前庭陣發(fā)癥占頭暈專病門診就診患者的3.2%[4]。臨床醫(yī)師接觸前庭陣發(fā)癥較少,對該病認識相對不足,因此誤診率較高,尤其在基層醫(yī)院。本文報道的11例患者中,入院后首次診斷均不準確,明確診斷為前庭陣發(fā)癥的時間平均>1周,其中8例為藥物治療好轉(zhuǎn)后反推確診。面對該病的診療現(xiàn)狀,其誤診原因除臨床醫(yī)師對前庭陣發(fā)癥認識不足之外,前庭陣發(fā)癥的臨床癥狀不典型、缺乏可以明確診斷的特異性實驗室檢查也是誤診原因之一。
前庭陣發(fā)癥的常見臨床表現(xiàn)為反復(fù)發(fā)作的短暫性眩暈,且體位變化可誘發(fā)癥狀發(fā)作,發(fā)作形式非常類似BPPV。本文中有5例患者初次診斷為BPPV,建議遇到體位誘發(fā)試驗結(jié)果不典型、手法復(fù)位效果不佳的患者,需警惕前庭陣發(fā)癥的可能。一般情況下,聽力下降或耳鳴的患者易被誤診為梅尼埃病、突發(fā)性耳聾,可以結(jié)合電測聽和BAEP檢查進行鑒別診斷。李艷成等[5]對51例前庭陣發(fā)癥患者的BAEP結(jié)果進行回顧性分析,發(fā)現(xiàn)前庭陣發(fā)癥患者BAEP異常率較高,且以Ⅰ~Ⅲ波峰間期延長為主,Ⅰ~Ⅲ波峰間期延長或其耳間差延長均提示蝸神經(jīng)受累,且病程越長,Ⅰ~Ⅲ波峰間期及其耳間差延長越明顯,蝸神經(jīng)損害越不可逆,并提出BAEP有助于診斷和評價前庭陣發(fā)癥的嚴重程度。臨床中多數(shù)疾病可引發(fā)患者聽力損害,因此遇到聽力損害的患者建議耳鼻喉科會診以進行鑒別診斷。眩暈患者常伴焦慮情緒,而精神心理相關(guān)性眩暈、頭暈臨床較常見,故前庭陣發(fā)癥易被誤診為焦慮狀態(tài)??菇箲]和鎮(zhèn)靜治療亦能緩解部分患者的臨床癥狀,因此易使臨床醫(yī)師堅持錯誤的診斷。筆者認為精神心理相關(guān)性眩暈應(yīng)作為排他性診斷,臨床診斷不能先入為主,尤其是抗焦慮治療效果不佳時,應(yīng)考慮診斷的準確性?;颊咴谘灠l(fā)作時不適感較強,因此不能準確自述,甚至對醫(yī)師詳細問診有抵觸和反感情緒,因此臨床醫(yī)生應(yīng)注意安撫,使患者配合問診。
前庭陣發(fā)癥的發(fā)病機制尚未明確,可能由前庭蝸神經(jīng)與血管交互壓迫引起。Hüfner等[3]研究結(jié)果顯示,95%的前庭陣發(fā)癥患者存在神經(jīng)與血管交互壓迫,李艷成等[6]對51例前庭陣發(fā)癥患者采用MRI三維穩(wěn)態(tài)進動快速成像序列(3D-FIESTA)對橋小腦角區(qū)軸位掃描,結(jié)果顯示42例患者存在神經(jīng)與血管交互壓迫,其中單側(cè)37例,雙側(cè)5 例。李慧等[7]采用三維-磁共振血管成像技術(shù)分別對28例前庭陣發(fā)癥及對照組患者進行掃描,結(jié)果顯示前庭陣發(fā)癥患者神經(jīng)與血管交互壓迫發(fā)生率高,且壓迫血管以小腦前下動脈多見。本文中6例患者發(fā)現(xiàn)前庭蝸神經(jīng)與血管交互壓迫,檢出率較低,分析原因為:(1)MRI普通平掃檢出率較低,建議采用局部薄層掃描以增加檢出率;(2)1.5T MRI分辨率較低,建議使用高分辨率MRI;(3)臨床醫(yī)生未能識別。本文3例患者在明確診斷后再次閱片發(fā)現(xiàn)前庭蝸神經(jīng)與血管交互壓迫,因此提高臨床醫(yī)生對前庭陣發(fā)癥的鑒別診斷意識意義重大。
臨床治療前庭陣發(fā)癥首選卡馬西平[3],對于卡馬西平不耐受的患者可以選用奧卡西平、加巴噴汀、丙戊酸或苯妥英鈉[8]。Russell等[9]研究結(jié)果顯示,低劑量加巴噴汀(600 mg/d)對前庭陣發(fā)癥有較好的控制效果。
綜上所述,前庭陣發(fā)癥的臨床癥狀以發(fā)作性眩暈、頭暈為主,磁共振檢查多顯示前庭蝸神經(jīng)與血管交互壓迫,BAEP檢查結(jié)果多顯示Ⅰ~Ⅲ波峰間期延長;前庭陣發(fā)癥的臨床誤診率高的原因與臨床醫(yī)生認識不足、患者病史提供不準確、臨床癥狀缺乏特異性、缺少高效特異的實驗室檢查手段有關(guān)。因此,快速明確診斷前庭陣發(fā)癥需加強臨床醫(yī)師對前庭陣發(fā)癥臨床特點的了解,從而減輕患者的經(jīng)濟、精神負擔(dān)。
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(本文編輯:毛亞敏)
Clinical Features and Causes of Misdiagnosis of Vestibular Paroxysmia
KONGWei-guo.
DepartmentofNeurology,thePeople′sHospitalofXuancheng,Xuancheng242000,China
ObjectiveTo analyze the clinical features and causes of misdiagnosis of vestibular paroxysmia.MethodsA total of 11 outpatients and inpatients were selected in the People′s Hospital of Xuancheng,and their clinical data was retrospectively analyzed,clinical features and causes of misdiagnosis summarized.Results(1)Clinical symptoms:10 cases performed as episodic vertigo and dizziness,4 cases performed as tinnitus,3 cases performed as instability of gait,2 cases performed as dysacusis;10 cases complicated with nausea,emesis and epigastric discomfort.Self-reported symptoms duration:6 cases within 10 minutes,3 cases from 10 minutes to 1 hour,2 cases over 1 hour.Symptoms attack frequency:10 to 50 times per month.Physical examination at attack showed that,11 cases performed as nystagmus,that mainly were horizontal nystagmus without any other abnormal signs of nervous system.Magnetic resonance inspection(MRI)found 6 cases with interactive oppression of vestibulocochlear nerve and blood vessel;electro-audiometry found 5 cases with dysacusis,including 4 cases with monaural dysacusis and 1 case with binaural dysacusis,thereinto 3 cases were mild,1 case was obvious.Brainstem auditory evoked potential(BAEP)examination found 6 cases with latency of Ⅰ to Ⅲ inter-peak.Diagnosis,treatment and misdiagnosis:5 cases were firstly diagnosed as benign paroxysmal positional vertigo(BPPV)and were treated by manual reposition;2 cases were firstly diagnosed as anxiety and were treated by anti-anxiety treatment;1 case was firstly diagnosed as posterior circulation ischemia(PCI),1 case was firstly diagnosed as cerebral insufficiency,both of them were treated by prevention of stroke and improvement of blood circulation;1 case was firstly diagnosed as sudden deafness and was treated by expansion of blood vessel and nutrition of nerve;1 case was firstly diagnosed as Meniere′s disease and was treated by diuresis and nutrition of nerve.The duration between first diagnosis and final definite diagnosis was 3 to 10 days,average at(7.2±2.1)days.Of the 11 cases,3 cases clarified a diagnosis according to clinical symptoms and laboratory examination,other 8 cases clarified a diagnosis according to the effectiveness of antiepileptic drugs combined with medical history,all of their clinical symptoms relieved to varying degrees.ConclusionEpisodic vertigo and dizziness are the main clinical symptoms of vestibular paroxysmia,MRI mostly showed interactive oppression of vestibulocochlear nerve and blood vessel,BAEP examination mostly showed latency of Ⅰ to Ⅲ inter-peak;the misdiagnosis rate is relatively higher,the causes of misdiagnosis includes insufficient understanding of clinicians,patient-provide inaccurate medical history,nonspecific clinical symptoms and laboratory examination methods.
Vestibular paroxysmia;Vertigo;Diagnostic errors
242000安徽省宣城市人民醫(yī)院神經(jīng)內(nèi)科
R 764.34
B
10.3969/j.issn.1008-5971.2016.02.032
2015-12-05;
2016-02-03)